I am confused that while researching about unsaturated fat, some sources say it is anti-inflammatory, while some sources say it is associated with inflammation. Does it still have mixed results or am I reading it wrong?


  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7160296/

In vitro experiments using acinar cells of the pancreas have shown that unsaturated fatty acids (UFAs) are associated with inflammation and necrosis, while saturated fatty acids (SFAs) are not harmful.

  1. https://www.nature.com/articles/nrgastro.2011.224

In vitro studies confirmed UFAs as the causative agent of this damage; UFAs were proinflammatory, impaired acinar cell function, inhibited mitochondria and induced cell death. No such effects were observed with saturated fatty acids.

  1. https://medicalxpress.com/news/2021-02-saturated-fats-severity-pancreatitis.html

Prior research has suggested people would be healthier if they reduced saturated fat consumption and ate more unsaturated fats—saturated fat has been associated with heart disease and obesity. Researchers have reported exceptions to this rule, however, which has led to the obesity paradox. ... The researchers found that patients who ate diets heavy in saturated fats who also developed pancreatitis experienced less severe symptoms than patients who ate a diet with more unsaturated fats.

  1. https://dash.harvard.edu/handle/1/34268572

Although omega-3 polyunsaturated fatty acids (n-3 PUFA) are known to have anti-inflammatory effects, the utility of these fatty acids in the alleviation of pancreatitis remained to be investigated. ... Our data provide evidence for a reduction of systemic inflammation in acute pancreatitis and of tissue fibrosis in chronic pancreatitis by increasing the tissue content of omega-3 polyunsaturated fatty acids.

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    +1. Welcome to the confusing world of research. Research regarding diet and inflammation in particular is riddled with contradictions. Any research regarding food over periods of time will be suspect because of built-in difficulties, especially if in vivo studies require participants to self-report. It's a mess. Wish I could answer your question, but the best I can do is to look at the studies very critically to see if they were well designed and carried out, how analysis was done, and keep an open mind. Remember the decades when butter and eggs were forbidden? I do. Commented Oct 6, 2023 at 16:28
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    Specific to your question, it's got problems. Your first quote is not the (in vivo retrospective study) researcher's observation but, but a repetition of someone else's (in vitro) conclusion; the second link is not to a study at all, but a summary of one; the third also isn't a study, and the fourth is just an abstract, meaning none of what you've quoted can be scrutinized at all from your links. So no real help can be given from what you've posted in your question. You need the originals. Commented Oct 6, 2023 at 16:45

1 Answer 1



No, you don't need to favor saturated fats in the hopes that if you do suffer from acute pancreatitis in the future, the overall harm will be slightly less severe. Your supporting links all focus on pancreatitis, and to focus solely on this pathological condition, we are already discussing about a minority. When we also take into account that the pancreatitis we are talking about is the one that is caused due to very high levels of fat in your blood (hypertriglyceridemia-induced pancreatitis), we are talking about even fewer individuals, who are already in a diseased state anyway.

In short, supporting the consumption of saturated, over unsaturated fats, just to mitigate the degree of a hypothetical future bout of pancreatitis is like supporting cigarette smoking in order to avoid certain diseases (emphasis mine):

Tobacco use may confer a small degree of protection against a small number of diseases and conditions, described in the sections below. However, the evidence that tobacco consumption can prevent lives being lost to these diseases and conditions is limited and further mechanistic studies are required for causal inference (see Section 3.0.1).2 Further, the number of deaths that may be prevented by smoking pales into insignificance compared to the number of deaths it has been demonstrated to cause. It is estimated that in 2015–16 tobacco use prevented 79 deaths in Australia, a very low number compared to the 20,031 deaths caused by smoking in that same year.[i]3 On the basis of these figures, tobacco might be said to save about one life for every 250 deaths it causes. Moreover, there is nothing to suggest that possible protection conferred against one disease will stop a given smoker from developing another tobacco-caused disease. So, for example, an individual who may have avoided Parkinson’s disease due to his or her smoking still runs a significant risk of dying from heart disease, lung cancer, or any of the multiplicity of other tobacco-caused diseases. Equally, smoking does not prevent Parkinson’s disease in all smokers.

To very succinctly answer your question, it's not that simple, and different types of fat play different roles and participate in different pathways in different cells of different parts of the body. As you will see, the same type of fat may, directly, or indirectly, promote inflammation in certain situations, and inhibit it in others. There is no one-size-fits-all model to address the "benevolence" of each type of fat, all the more so, as "inflammation" is a relatively loaded term. Some are good for one thing, others are good for another thing, and certain ones are bad for a few things. We always have to consider the totality of the evidence, and be liberal in what we read, but conservative in what we conclude.

Long answer

The evidence you point to are only looking into how visceral fat composition affects the course of severe acute pancreatitis. If your question is: "Given a situation of acute pancreatitis, are unsaturated fatty acids linked to worse outcomes?", then your answer is yes:

In [1]:

In multivariable analysis, patients from regions with high UFA intake had a significantly increased frequency of local complications, persistent organ failure (POF), mortality, and moderate-to-severe disease in the model without obesity and a higher frequency of POF in the model with obesity. Patients from regions with high MUFA intake had significantly more local complications and moderate-to-severe disease; this significance remained for moderate-to-severe disease when obesity was added to the model

In [2]:

In vitro studies of pancreatic acinar cells showed that unsaturated fatty acids were proinflammatory, releasing intracellular calcium, inhibiting mitochondrial complexes I and V, and causing necrosis. Saturated fatty acids had no such effects

In [3]:

Lipolysis of unsaturated triglyceride and resulting unsaturated fatty acids (UFA) oleic and linoleic acids induced necro-apoptosis at less than half the concentration in NCs* but other agents did not do so at more than two times these concentrations.

*NCs: Necrotic Collections.

At this point, one should wonder (like you did), how come? There is an established fact that saturated fats generally cause more harm than unsaturated fats, is there an explanation for this "paradox"?

Well, in [4] it is described that:

We show that the higher likelihood of SAP* associates with a higher unsaturated triglyceride content in visceral fat. This occurs because the presence of SFAs in triglycerides makes the interaction of the substrate with PNLIP structurally and energetically unfavorable. Moreover, the unsaturated NEFA generated by lipolysis can exist as monomers (65) in aqueous media, unlike saturated NEFA*, resulting in injurious signaling, lipotoxic inflammation, and organ failure. This can potentially explain why higher dietary UFAs may result in worse AP in leaner animals and humans with lower BMIs compared to the more obese ones who consume a diet with higher proportions of saturated fat (Fig. 7), resulting in the obesity paradox.

*SAP: Severe acute pancreatitis.

What this tells us, is that pancreatic lipase (an enzyme that breaks down triglycerides, converting them into free fatty acids) is not very efficient at releasing saturated fatty acids from triglycerides (which are composed of three fatty acids, combined with glycerin). Unsaturated fatty acids are easier to release for pancreatic lipase, and a corresponding "flood" of unsaturated free (as in "freely floating around, unchained to glycerol in the form of mono-/di-/tri-glycerides") fatty acids (NEFAs) further spread inflammatory chaos.

*NEFA: Non-Esterified Fatty Acid (free fatty acid, not in a -glyceride form).

It is, indeed, further observed, in [5] (emphasis mine) that:

In conclusion, our in vitro results provide an explanation for the clinical observation that only a portion of HTG* patients develop AP* and that some patients with HTG seldom develop pancreatitis despite marked elevation of triglyceride level. Triglycerides were unable to induce an attack of AP. Only when triglycerides are hydrolyzed by lipase into FFAs and the concentration of unsaturated fatty acids is sufficiently high do acinar cells become injured, thereby resulting in pancreatitis.

*AP: Acute pancreatitis. *HTG: Hypertriglyceridemia.

It should be clear, to you, by now, that all we have actually argued for here is that unsaturated fatty acids are pro-inflammatory (i.e. they appear to promote further inflammation) solely in the context of hypertriglyceridemia-induced pancreatitis.

Can we generalise from this and go on to state that unsaturated fatty acids promote inflammation?


Of course not!

Scientists often ask themselves, just like every layperson-on-the-subject: "what should we make of the combined literature?". Well, there is a sizable body of literature supporting a well-established fact, that saturated fatty acids increase the risk of cardiovascular disease. The most recent Cochrane review that I could find on the subject states, specifically, in their Plain English Summary of the key results:

This means that, if 56 people without cardiovascular disease, or 53 people who already have cardiovascular disease, reduce their saturated fat for around 4 years, then one person will avoid a cardiovascular event (heart attack or stroke) they would otherwise have experienced.

While it is not wise to take most things without a grain of salt too literally, I am having a hard time avoiding the extrapolation of this ratio to the national levels, where a country with a population of 300 millions could avoid around 5 millions of cardiovascular events over 4 years. If you think this is too simplistic, the CDC actually tells us that every year, about 805,000 people in the United States have a heart attack. The CDC also tells us that every year, more than 795,000 people in the United States have a stroke. For better or for worse, after a huge amount of research, numbers do come into play and disease burden quantification is actually a thing.

In short, it is all about risk and benefit (it's always like this in medicine). There is a much greater benefit into avoiding saturated fats, than there is a risk, and if an individual has too high blood triglyceride levels, we are already into pathological condition territory, and that is what ought to be addressed.

[1] García-Rayado G, Varela-Moreiras G, Lanas Á, Ferrández Á, Balza-Lareu N, Cervera JI, Bodenlle-Bello MP, Argüelles-Arias AM, Latorre P, Udaondo-Cascante MA, Soria-de-la-Cruz MJ, Lariño-Noia J, García-Figueiras R, Gil-García-Ollauri C, Ituarte-Uriarte R, Rosales-Alexander CL, Soriano J, Rodríguez-Peláez M, Mesa-Álvarez A, Oblitas E, Menso MM, Bertoletti F, Rodríguez-Prada JI, Guzmán-Suárez S, Closa D, de-Madaria E. Dietary Fat Patterns and Outcomes in Acute Pancreatitis in Spain. Front Med (Lausanne). 2020 Apr 9;7:126. doi: 10.3389/fmed.2020.00126. PMID: 32328495; PMCID: PMC7160296.

[2] Navina S, Acharya C, DeLany JP, Orlichenko LS, Baty CJ, Shiva SS, Durgampudi C, Karlsson JM, Lee K, Bae KT, Furlan A, Behari J, Liu S, McHale T, Nichols L, Papachristou GI, Yadav D, Singh VP. Lipotoxicity causes multisystem organ failure and exacerbates acute pancreatitis in obesity. Sci Transl Med. 2011 Nov 2;3(107):107ra110. doi: 10.1126/scitranslmed.3002573. PMID: 22049070; PMCID: PMC3321362.

[3] Noel P, Patel K, Durgampudi C, Trivedi RN, de Oliveira C, Crowell MD, Pannala R, Lee K, Brand R, Chennat J, Slivka A, Papachristou GI, Khalid A, Whitcomb DC, DeLany JP, Cline RA, Acharya C, Jaligama D, Murad FM, Yadav D, Navina S, Singh VP. Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections. Gut. 2016 Jan;65(1):100-11. doi: 10.1136/gutjnl-2014-308043. Epub 2014 Dec 10. PMID: 25500204; PMCID: PMC4869971.

[4] Biswajit Khatua et al. Adipose saturation reduces lipotoxic systemic inflammation and explains the obesity paradox. Sci. Adv. 7, eabd6449 (2021).doi: 10.1126/sciadv.abd6449

[5] Chang YT, Chang MC, Tung CC, Wei SC, Wong JM. Distinctive roles of unsaturated and saturated fatty acids in hyperlipidemic pancreatitis. World J Gastroenterol. 2015 Aug 28;21(32):9534-43. doi: 10.3748/wjg.v21.i32.9534. PMID: 26327761; PMCID: PMC4548114.

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    Your level of detail really blew my mind, glad to have you in this community, I learnt a great deal, thank you! Commented Oct 9, 2023 at 0:23
  • @user1589188 you are most welcome! I probably got a little bit carried away in my answer, I really hope it doesn't look too much of a rant, but, among other things, more like an honest effort to prevent and tackle potential misunderstandings on the subject. Thank you too, for a truly interesting question! Commented Oct 9, 2023 at 2:59

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